Radio Electric Asymmetric Conveyer Technology Modulates Neuroinflammation in a Mouse Model of Neurodegeneration.
10.1007/s12264-017-0188-0
- Author:
Maria Antonietta PANARO
1
;
Alessandra ALOISI
2
;
Giuseppe NICOLARDI
3
;
Dario Domenico LOFRUMENTO
4
;
Francesco DE NUCCIO
3
;
Velia LA PESA
5
;
Antonia CIANCIULLI
1
;
Rosaria RINALDI
2
;
Rosa CALVELLO
1
;
Vania FONTANI
6
;
Salvatore RINALDI
6
Author Information
1. Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy.
2. CNR Institute for Microelectronics and Microsystems, Via Monteroni (Campus Ecotekne), 73100, Lecce, Italy.
3. Department of Biological and Environmental Sciences and Technologies, Section of Human Anatomy, University of Salento, Lecce, Italy.
4. Department of Biological and Environmental Sciences and Technologies, Section of Human Anatomy, University of Salento, Lecce, Italy. dario.lofrumento@unisalento.it.
5. Neuropathology Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, 20132, Milan, Italy.
6. Department of Regenerative Medicine, Rinaldi Fontani Institute, Viale Belfiore 43, 50144, Florence, Italy.
- Publication Type:Journal Article
- Keywords:
Neurodegeneration;
Neuroinflammation;
Parkinson’s disease;
REAC TO-RGN-N treatment
- MeSH:
Animals;
Corpus Striatum;
pathology;
Electric Stimulation;
methods;
Inflammation;
pathology;
Male;
Mice;
Nerve Degeneration;
pathology;
Nerve Regeneration;
physiology;
Parkinsonian Disorders;
pathology
- From:Neuroscience Bulletin
2018;34(2):270-282
- CountryChina
- Language:English
-
Abstract:
In this study, the effects of Radio Electric Asymmetric Conveyer (REAC), a non-invasive physical treatment, on neuroinflammatory responses in a mouse model of parkinsonism induced by intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), were investigated in vivo. We found that the REAC tissue optimization treatment specific for neuro-regenerative purposes (REAC TO-RGN-N) attenuated the inflammatory picture evoked by MPTP-induced nigro-striatal damage in mice, decreasing the levels of pro-inflammatory molecules and increasing anti-inflammatory mediators. Besides, there was a significant reduction of both astrocyte and microglial activation in MPTP-treated mice exposed to REAC TO-RGN-N. These results indicated that REAC TO-RGN-N treatment modulates the pro-inflammatory responses and reduces neuronal damage in MPTP-induced parkinsonism.
